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长期吸入镍纳米颗粒会加剧易感小鼠模型的动脉粥样硬化。

Long-term inhalation exposure to nickel nanoparticles exacerbated atherosclerosis in a susceptible mouse model.

机构信息

Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York, USA.

出版信息

Environ Health Perspect. 2011 Feb;119(2):176-81. doi: 10.1289/ehp.1002508. Epub 2010 Sep 22.

DOI:10.1289/ehp.1002508
PMID:20864429
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3040603/
Abstract

BACKGROUND

Because associations have been reported between inhaled ambient ultrafine particles and increased risk of cardiopulmonary disease, it has been suggested that inhaled engineered nanoparticles (NPs) may also induce adverse effects on the cardiovascular system.

OBJECTIVE

We examined the long-term cardiovascular effects of inhaled nickel hydroxide NPs (nano-NH) using a sensitive mouse model.

METHODS

Hyperlipidemic, apoprotein E-deficient (ApoE-/-) mice were exposed to nano-NH at either 0 or 79 μg Ni/m3, via a whole-body inhalation system, for 5 hr/day, 5 days/week, for either 1 week or 5 months. We measured various indicators of oxidative stress and inflammation in the lung and cardiovascular tissue, and we determined plaque formation on the ascending aorta.

RESULTS

Inhaled nano-NH induced significant oxidative stress and inflammation in the pulmonary and extrapulmonary organs, indicated by up-regulated mRNA levels of certain antioxidant enzyme and inflammatory cytokine genes; increased mitochondrial DNA damage in the aorta; significant signs of inflammation in bronchoalveolar lavage fluid; changes in lung histopathology; and induction of acute-phase response. In addition, after 5-month exposures, nano-NH exacerbated the progression of atherosclerosis in ApoE-/- mice.

CONCLUSIONS

This is the first study to report long-term cardiovascular toxicity of an inhaled nanomaterial. Our results clearly demonstrate that long-term exposure to inhaled nano-NH can induce oxidative stress and inflammation, not only in the lung but also in the cardiovascular system, and that this stress and inflammation can ultimately contribute to progression of atherosclerosis in ApoE-/- mice.

摘要

背景

由于吸入环境超细颗粒与心肺疾病风险增加有关，因此有人认为吸入工程纳米颗粒（NPs）也可能对心血管系统产生不良影响。

目的

我们使用敏感的小鼠模型研究了吸入镍氢氧化物纳米颗粒（nano-NH）的长期心血管影响。

方法

高脂血症、载脂蛋白 E 缺陷（ApoE-/-）小鼠通过全身吸入系统暴露于 0 或 79μgNi/m3 的 nano-NH，每天 5 小时，每周 5 天，暴露时间为 1 周或 5 个月。我们测量了肺和心血管组织中氧化应激和炎症的各种指标，并确定了升主动脉上斑块的形成。

结果

吸入的 nano-NH 诱导了肺部和肺外器官的显著氧化应激和炎症，表现为某些抗氧化酶和炎症细胞因子基因的 mRNA 水平上调；主动脉中线粒体 DNA 损伤增加；支气管肺泡灌洗液中明显的炎症迹象；肺组织病理学变化；以及急性期反应的诱导。此外，经过 5 个月的暴露，nano-NH 加剧了 ApoE-/-小鼠动脉粥样硬化的进展。

结论

这是第一项报道吸入纳米材料长期心血管毒性的研究。我们的结果清楚地表明，长期吸入 nano-NH 可引起氧化应激和炎症，不仅在肺部，而且在心血管系统中，这种应激和炎症最终可能导致 ApoE-/-小鼠动脉粥样硬化的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/e038afcdb80c/ehp-119-176f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/4c23573cb7ee/ehp-119-176f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/3a9a3513b6bf/ehp-119-176f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/5b62684d9793/ehp-119-176f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/1f05047b7f98/ehp-119-176f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/e038afcdb80c/ehp-119-176f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/4c23573cb7ee/ehp-119-176f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/3a9a3513b6bf/ehp-119-176f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/5b62684d9793/ehp-119-176f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/1f05047b7f98/ehp-119-176f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1de4/3040603/e038afcdb80c/ehp-119-176f5.jpg

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